中文摘要：

背景尽管CD4+ T 房间 apoptosis 和CD8+ T 房间回答广泛地在 HIV 感染期间被学习了， apoptosis 怎么发信号，在房间仍然需要是在场的 elucidated.The 的CD4+ T 被开始学习被设计描绘功能未知的基因， C6orf120 ，并且阐明它在 导致tunicamycin 的CD4+ T apoptosis.Methods 的主要角色编码顺序的 C6orf120 从外部血 mononuclear 房间( PBMC )被放大爱滋病 patients.The DNA 碎片的全部的 RNA 被插入

英文摘要：

Background Although CD4＋ T cell apoptosis and CD8＋ T cell responses have been extensively studied during HIV infection, how apoptosis signals being initiated in CD4＋ T cells still need to be elucidated. The present study was designed to characterize the function-unknown gene, C6orf120, and elucidates its primary role in tunicamycin-induced CD4＋ T apoptosis. Methods The C6orf120 coding sequence was amplified from peripheral blood mononuclear cells （PBMCs） total RNA of AIDS patients. The DNA fragment was inserted into the pET-32a expression system, transformed into Escherichia coli, and preparation of C6ORF120 recombinant protein. The magnetic cell separation technology was used to prepare primary CD4＋ T cells and CD8＋T cells. The primary T cells were cultured at 1×10^6 cells/ml, treated with 0, 0.1,1, 10, 100 and 200 ng/ml of C6orf120 recombinant protein for 48 hours, then harvested for cell cycle and apoptosis analysis. Tunicamycin （0.5 μmol/L） was used to induce endoplasmic reticulum stress in Jurkat cells. The biomarker 78 KDa glucose-regulated protein （GRp78） and growth arrest and DNA damage （GADD） were used to evaluate endoplasmic reticulum stress of Jurkat cells. Results We prepared C6ORF120 recombinant protein and its polyclonal antibody. Immunohistochemical analysis showed that C6orf120 mainly expressed in hepatocytes and cells in germinal center of lymph node. At concentration of 0.1, 1, 10, 100, and 200 ng/ml, C6orf120 recombinant protein could induce apoptosis of Jurkat cells and primary CD4＊T cells, and promoting G2 phase of its cell cycle. Western blotting analysis showed that C6ORF120 recombinant protein increased the expression of GRp78 and GADD in Jurkat cells in vitro. Conclusion Our results suggested that C6ORF120 could induce apoptosis of CD4＋ T cells, at least in part, mediated with endoplasmic reticulum stress.